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Papers: 18 May 2024 - 24 May 2024

2024 May 14

Biochem Biophys Res Commun



Hericenone C attenuates the second phase of formalin-induced nociceptive behavior by suppressing the accumulation of CD11c-positive cells in the paw epidermis via phosphorylated P65.


Li J, Hamamura K, Yoshida Y, Kawano S, Uchinomiya S, Xie J, Scuteri D, Fukuoka K, Zaitsu O, Tsurusaki F, Terada Y, Tsukamoto R, Nishi T, Fukuda T, Oyama K, Bagetta G, Ojida A, Shimizu K, Ohdo S, Matsunaga N


Hericenone C is one of the most abundant secondary metabolites derived from Hericium erinaceus, under investigation for medicinal properties. Here, we report that Hericenone C inhibits the second phase of formalin-induced nociceptive behavior in mice. As the second phase is involved in inflammation, in a mechanistic analysis on cultured cells targeting NF-κB response element (NRE): luciferase (Luc)-expressing cells, lipopolysaccharide (LPS)-induced NRE::Luc luciferase activity was found to be significantly inhibited by Hericenone C. Phosphorylation of p65, which is involved in the inflammatory responses of the NF-κB signaling pathway, was also induced by LPS and significantly reduced by Hericenone C. Additionally, in mice, the number of CD11c-positive cells increased in the paw during the peak of the second phase of the formalin test, which decreased upon Hericenone C intake. Our findings confirm the possibility of Hericenone C as a novel therapeutic target for pain-associated inflammation.